The fruitfly Drosophila melanogaster is one of the best genetic model organisms for a large number of research areas in modern biology. However , one of the most useful genetic tools has been prominently missing for Drosophila, that is the ability to target specific genes for mutation by homologous recombination. Gene targeting has, for over twenty years, allowed yeast and mouse researchers to introduce specific mutations to essentially any gene. Such a tool is especially important for gene function studies in organisms with a completely sequenced genome. Dr. Rong was the main driving force for the recent development of a gene targeting method in Drosophila. Such method has allowed Drosophila researchers worldwide to successfully mutate many different loci that were not previously identified in traditional mutant screens. As a demonstration of the general applicability of the method, Dr. Rong knocked out the Drosophila homolog of the tumor suppressor p53 in collaboration with Dr. Gerald Rubin's group. Characterization of the mutant phenotype of the Drosophila mutant is in progress. The main research interest of Dr. Rong's group is to study the mechanisms for DNA double strand break repair in Drosophila. To facilitate such a study, Dr. Rong has introduced a site-specific double strand break system into Drosophila in which one can control the position of the break, the number of breaks, the timing of breakage, and the genomic environment surrounding the break. Using this system, Dr. Rong was able to provide evidence suggesting that genomic structure around the DNA break dictates the choice of not only the repair mechanism but also the template for repair. A goal of the lab is to combine the power of the site-specific breakage system and the gene targeting method to elucidate the function of gene products involved in the repair of these DNA lesions. The work of Dr. Rong's group would contribute to a better understanding of how eukaryotic organisms maintain the physical integrity of their genomes.